The studies of our laboratory focus on the molecular mechanism of tumor metastasis in breast and prostate cancers. Although the overall incidence of these cancers is gradually declining, more than 90% of cancer death is still attributable directly to the metastatic disease. Therefore, understanding the pathological mechanism of metastatic process is urgently needed in order to identify better therapeutic targets of this devastating disease. Our lab is working on the following four key areas, by particularly focusing on tumor microenvironment, cancer stem cells and non-coding RNAs.

Tumor microenvironment of metastasis in the bone and the brain

Tumor metastasis occurs in a relatively organ-specific manner, and the tumor microenvironment in each organ plays important roles. Our research particularly focuses on both brain and bone metastasis of breast and prostate cancers. We identified specific components of host cells in these organs and clarified signaling networks in cancer stem cells and microenvironmental cells, which led to discoveries of several novel therapeutic targets and small molecules for potential clinical use.
Selected publications:

Roles of microRNAs in tumor progression

MicroRNAs play critical roles in tumor progression at various stages. We are particularly interested in the roles of microRNAs in cancer stem cells in tumor metastasis. Our results revealed that different microRNAs promote metastasis of cancer stem cells in organ and stage specific manners. We also clarified how the expressions of these microRNAs are regulated through interaction with microenvironmental cells.
Selected publications:

Fatty acid metabolism in tumor initiation and progression

Fatty acid synthesis plays a pivotal role in tumor initiation and progression by providing energy and cell membrane components to rapidly growing cancer cells. De novo synthesis of lipid is quite specific to cancer cells and blocking this process induces apoptosis to them. Thus the fatty acid synthase (FAS) is considered to be an excellent therapeutic target. In a series of publications, we reported (i) how FAS expression is regulated, (ii) what is the role of FAS in cancer stem cells, and (iii) molecular mechanism of FAS-mediated apoptosis. Our finding led to discoveries of additional targets in this pathway and provided a strong rationale for using FAS pathway inhibitors for the treatment of both early and late stages of cancer as well as recurrence disease.
Selected publications:

Identification of tumor metastasis suppressor genes and elucidating their functions

The existence of tumor metastasis suppressor genes was long been predicted and they were expected to suppress only metastatic process but not tumor initiation. We identified several chromosomal regions of metastasis suppression in prostate and breast cancers. We also clarified the function of two key metastasis suppressor genes, KAI1 and NDRG1, their signaling pathways and mechanism by which they cross-talk each other. We then showed several small molecules that potentially activate these genes and suppress recurrence.
Selected publications: